The roles of PKC-δ and PKC-ε in myocardial ischemia/reperfusion injury

Ischemia and reperfusion (I/R) cause a reduction in arterial blood supply to tissues, followed by the restoration of perfusion and consequent reoxygenation. The reestablishment of blood flow triggers further damage to ischemic tissue through reactive oxygen species (ROS) accumulation, interference with cellular ion homeostasis, opening of mitochondrial permeability transition pores (mPTPs) and promotion of cell death (apoptosis or necrosis). PKC-delta and PKC-epsilon, belonging to a family of serine/threonine kinases, have been demonstrated to play important roles during I/R injury in cardiovascular diseases. However, the cardioprotective mechanisms of PKC-delta and PKC-epsilon in I/ R injury have not been elaborated until now. This article discusses the roles of PKC-delta and PKC-epsilon during myocardial I/R in redox regulation (redox signaling and oxidative stress), cell death (apoptosis and necrosis), Ca2+ overload, and mitochondrial dysfunction.

Automated summary

PKC-delta and PKC-epsilon play crucial roles in protecting the myocardium during ischemia/reperfusion injury through their involvement in redox regulation, cell death, Ca2+ overload, and mitochondrial dysfunction.